The objective of this training program is to provide superb training of bright, young physician-scientists to develop the necessary skills to conduct state-of-the-art basic and translational research in the field of nephrology. The emphasis of the program is to provide training in the experimental design, methodology, and analyses of research aimed at elucidating mechanisms of renal injury and scarring as it relates to renal diseases associated with hypertension, diabetes, glomerular disease, and other renal conditions. The ultimate goal is to train physician-scientists to become independent investigators in academic nephrology. To achieve this objective, a multidisciplinary program has been developed to provide individualized training to postdoctoral candidates. Selected candidates develop a research project in concert with both a Nephrology and Basic Science mentor and undertake a minimum of two and preferably 3 years of research in their respective laboratories. A strong didactic program is also provided to ensure teaching in experimental design, molecular biologic methodology, biostatistics, and ethics. The emphasis of the program centers on several major areas of renal inflammation and fibrosis. These include the role of effector cells (macrophages and T cells) and their mechanisms of recruitment and dispersal, including the biology of chemokines, leukocyte adhesion molecules, the Slit/Robo chemorepellant molecules, monocyte/macrophage migration inhibition factor, and macrophage activation, proliferation and apoptosis. The cellular mechanisms involved in the renal response to injury will also be studied in detail, including the role of impaired angiogenesis, tubular apoptosis, and mechanisms of fibrosis. The latter includes the role of cytokines (IL-1beta and TNFalpha), TGF-beta/Smad signaling, the role of MAP kinases, and of the ubiquitination/proteasomal system in cytokine receptor degradation and cytokine unresponsiveness. Additional emphasis is placed on mechanisms of smooth muscle cell injury and proliferation in the kidney, particularly as it relates to the development of hypertension, and the various biochemical (such as uric acid) and vasoactive mediators (such as stanniocalcin) that influence smooth muscle cell proliferation, migration, hypertrophy and contraction. The interdisciplinary, multi-faceted plan integrates several important fields (biochemistry, immunology, physiology and pathology) to dissect structure function relationships linking basic cellular signaling and molecular mechanisms with translational research in animal models of disease.